DETAILED ACTION
This action is in reply to papers filed 2/2/2026. Claims 1-4 and 6-20 are pending and examined herein.
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Examiner’s Note
All paragraph numbers throughout this office action, unless otherwise noted, are from the as-filed specification of this application.
Maintained Rejection(s)
The 103 (a) rejection of claims 1-4 and 6-20 as being unpatentable over Conway et al. (PgPub US20150056705A1, Filed 5/15/2014), Liu et al. (PgPub US20150071903A1, Filed 8/18/2014), Negre et al. (PgPub US20150203868A1, Filed 9/23/2011), Hoge et al. (PgPub US20160367702A1, Filed 7/11/2014), and Zhang (PgPub US20140357530A1, Filed 8/19/2014)is maintained. Applicant’s arguments will be addressed following the maintained rejection.
The nonstatutory double patenting rejection of claims 1-4 and 6-20 as being unpatentable over claims 35-46 and 49-57 of copending Application No. 15619737 (reference application) is maintained. No specific argument was presented by Applicant.
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Claim(s) 1-4 and 6-20 remain rejected under 35 U.S.C. 103 as being unpatentable over Conway et al. (PgPub US20150056705A1, Filed 5/15/2014), Liu et al. (PgPub US20150071903A1, Filed 8/18/2014), Negre et al. (PgPub US20150203868A1, Filed 9/23/2011), Hoge et al. (PgPub US20160367702A1, Filed 7/11/2014), and Zhang (PgPub US20140357530A1, Filed 8/19/2014).
Regarding claim 1, Conway teaches a method of modifying an endogenous gene, such as the B-cell lymphoma/leukemia 11A (BCL11A) gene (as in claim 7) or the PD1 gene (as in claim 9) (Pgs. 2-3, para. 22), the method comprising administering to a hematopoietic stem cell (as further in claim 1) (Pg. 3, para. 23-24) a first nucleic acid molecule comprising a chimeric (as in claim 14) single guide RNA (Pg. 5-6, para. 46-50; Pg. 15, para. 93) that recognizes a target site in the endogenous gene and a second nucleic acid molecule, that encodes a functional domain, wherein the functional domain, such as a mutated Cas9 nickase (as in claim 10) (see claim 3 of Conway; Pg. 3, para. 25), associates with the single guide RNA on the target site, thereby modifying the endogenous gene (Pgs. 2-3,para. 22). Conway teaches that by “single guide RNA” they refer to the polynucleotide sequence comprising the guide sequence, the tracr sequence and the tracr mate sequence (as in further in claim 1) (Pg. 15, para. 93). Conway explains that the CRISPR-Cas nuclease creates a double-stranded break in the target sequence (e.g., cellular chromatin) at a predetermined site, and a “donor” polynucleotide, having homology to the nucleotide sequence in the region of the break (i.e. HDR template), can be introduced into the cell (as in claim 4) (Pg. 7, para. 57; Pg. 25, para. 181). Conway teaches the modified cells can then administered to the human patient (as in claim 19) (Pg. 20, para. 142) following mild myeloablative pre-conditioning (as in claim 2) (Pg. 3, para. 24), for purposes of treatment. In one embodiment, Conway teaches the treatment is for β-thalassemias (as in claim 6) (Pg. 5, para. 45-47).
However, Conway fails to teach a particle comprising pre-annealed complex comprising CRISPR-Cas9 protein and one or more single guide RNA molecules (as further in claim 1).
Before the effective filing date of the claimed invention, Liu et al. taught nanoparticle (as in claim 1, in-part) formulations have enabled efficient encapsulation and delivery of nucleic acids, while avoiding non-specific electrostatic interactions and consequent sequestration. However, Liu notes that proteins are chemically diverse, and therefore unlike highly anionic nucleic acids, liposomal formulations have not been similarly successful for the efficient delivery of proteins. For example, while proteins can be encapsulated non-specifically and delivered by rehydrated lipids in vitro, the efficacy of encapsulation is dependent on protein concentration and is generally inefficient, and thus has not seen widespread application. Thus, Liu teaches aspects of the present disclosure relate to the recognition that anionic proteins or protein complexes (including those proteins associated with nucleic acids) may be able to take advantage of the same electrostatics-driven encapsulation used by cationic liposomal reagents for nucleic acid delivery. While few proteins natively possess the density of negative charges found in the phosphate backbone of nucleic acids, translational fusion to, or non-covalent association with, an anionic carrier such as a negatively supercharged protein or a nucleic acid as described herein render the resulting effector protein or protein complex sufficiently anionic to drive efficient encapsulation of such protein cargoes by cationic liposomal reagents (Pg. 19, para. 129).
Thus, towards this end, Liu teaches a composition comprising a Cas9 protein and a cationic lipid (as further in claim 1 and as in claim 16), wherein the Cas9 protein is associated with a gRNA, and the composition is capable of delivering the Cas9 protein to the interior of a cell (Pg. 20, para. 132). For delivery of Cas9:sgRNA complexes, Liu teaches 1 μL of 200 μM Cas9 protein was mixed with 2 μL of 100 μM sgRNA (which reads on a ‘pre-annealed complex ’ as recited in claim 1) and incubated for 5 minutes at room temperature before mixing with 3 μL of either RNAiMAX or Lipofectamine 2000 and incubating for an additional 30 minutes prior to injection (Pg. 51, para. 240). In some embodiments, Liu teaches the complex is further combined with a pharmaceutically acceptable carrier or excipient such as natural polymers or synthetic polymers (Pg. 43, para. 173). Liu further notes that formulations suitable for buccal administration may comprise a powder and/or an aerosolized and/or atomized solution and/or suspension comprising active ingredient. Such powdered, aerosolized, and/or aerosolized formulations, when dispersed, may have an average particle (as in claim 1, in-part) and/or droplet size in the range from about 0.1 nm to about 200 nm and may further comprise one or more of any additional ingredients described herein (Pg. 47, para. 209). Continuing, Liu teaches that in some embodiments, a cell treated with a functional effector protein according to the strategies or methods disclosed herein, or the progeny of such a cell, is used in a cell-replacement therapeutic approach, whereby the treated cells are administered to the subject from which the somatic cell was obtained (as in claim 2 and claim 3) (Pg. 42, para. 164). Notably, Liu teaches suitable cells include human cells, stem cells, progenitor cells, and blood cells (Pg. 14, para. 98).
However, neither Conway nor Liu teaches the cells are CD34+, CD59+, Thy1/CD90+, CD38lo/−, C-kit/CD117+, and Lin(−) hematopoietic stem cells (as in claim 13).
Before the effective filing date of the claimed invention, Negre et al. relate to improved gene therapy compositions for expanding hematopoietic cells (as further in claim 1) and related methods for treatment of diseases, disorders, and conditions of the hematopoietic system (Pg. 1, para. 3). In particular, Negre teaches the compositions of the present invention may be formulated for delivery encapsulated in a lipid particle (Pg. 20, para. 318). Negre teaches the transduced cells are human HSCs characterized as CD34+, CD59+, Thy1/CD90+, CD38lo/−, C-kit/CD117+, and Lin(−) (as further in claim 1 and as in claim 13). Additionally, Negre teaches, for human HSCs, CD133 may represent an early marker, as both CD34+ and CD34− HSCs have been shown to be CD133+ (as in claim 20) (Pg. 22, para. 339).
However, none of Conway, Liu and Negre teach the particle comprises a lipid nanoparticle comprising a cationic lipid, cholesterol, and a polyethylene glycol (PEG)-containing lipid (as in claim 1).
Before the effective filing date, Hoge et al. taught methods of using synthetic polynucleotides, e.g., modified mRNA, encoding CRISPR related proteins including dCAS9 and synthetic sgRNAs targeting a gene of interest (Abstract) in an ex vivo setting whereby the treated cells are hematopoietic cells (Pg. 48, para. 523). Hoge teaches the pharmaceutical compositions may be formulated in liposomes comprising 48% cholesterol, 2% PEG-c-DMA, and 30% cationic lipid (as further in claim 1) (Pg. 24, para. 281).
However, none of Conway et al., Liu et al., Negre et al. and Hoge et al. teach the genomic locus encodes or controls expression of PCSK9 (as in claim 8, the Cas9 is Streptococcus pyogenes Cas9 (SpCas9) (as in claim 11) or Streptococcus aureus Cas9 (SaCa9) (as in claim 12) or that the Cas9 comprises at least two NLSs (as in claim 15). Further, none of the aforementioned references teach mutations in a catalytic domain (as in claim 17), wherein the one or more mutations in the catalytic domain comprise, with reference to SpCas9, one or more of D10A, E762A, H840A, N854A, N863A and D986A (as in claim 18).
Before the effective filing date of the claimed invention, Zhang taught methods for using one or more elements of a CRISPR-Cas system (Pg. 2, para. 13). In one embodiment, Zhang teaches the CRISPR-Cas system targets PCSK9 (as in claim 8), a gene involved in hypercholesterolemia (Pg. 75,para. 616; Pg. 77, para 642). In a preferred embodiment, Zhang teaches the Cas enzyme is wildtype Cas9 or any of the modified versions described herein, including any naturally-occurring bacterial Cas9 as well as any chimaeras, mutants, homologs or ortholog (Pg. 3, para. 21). Most preferably, the Cas9 enzyme is from, or is derived from saCas9 (as in claim 12) or spCas9 (as in claim 11) (Pg. 3, para. 23). In an aspect of the invention the CRISPR enzyme comprises one or more mutations in a catalytic domain, wherein the one or more mutations are selected from the group consisting of D10A, E762A, H840A, N854A, N863A and D986A (as in claim 17 and claim 18) (Pg. 6, para. 46). Continuing, Zhang hypothesized that the most effective Cas9 transcriptional modulator would be strongly localized to the nucleus where it would have its greatest influence on transcription. Moreover, any residual Cas9 in the cytoplasm could have unwanted effects. Zhang and colleagues determined that wild-type Cas9 does not localize into the nucleus without including multiple nuclear localization signals (NLSs) (as in claim 15) (Pg. 89, para. 931).
The combination of prior art cited above in all rejections under 35 U.S.C.103 satisfies the factual inquiries as set forth in Graham v. John Deere Co., 383 U.S. 1,148 USPQ 459 (1966). Once this has been accomplished the holdings in KSR can be applied (KSR International Co. v. Teleflex Inc. (KSR), 550 U.S. 389, 82 USPQ2d 1385 (2007): "Exemplary rationales that may support a conclusion of obviousness include: (A) Combining prior art elements according to known methods to yield predictable results; (B) Simple substitution of one known element for another to obtain predictable results; (C) Use of known technique to improve similar devices (methods, or products) in the same way; (D) Applying a known technique to a known device (method, or product) ready for improvement to yield predictable results; (E) "Obvious to try" - choosing from a finite number of identified, predictable solutions, with a reasonable expectation of success; (F) Known work in one field of endeavor may prompt variations of it for use in either the same field or a different one based on design incentives or other market forces if the variations are predictable to one of ordinary skill in the art; (G) Some teaching, suggestion, or motivation in the prior art that would have led one of ordinary skill to modify the prior art reference or to combine prior art reference teachings to arrive at the claimed invention."
In the present situation, rationales A and G are applicable. Before the effective filing date of the claimed invention, it would have been prima facie obvious to an artisan of ordinary skill to combine the teachings of Conway et al., wherein Conway teaches a method of modifying an endogenous gene in a hematopoietic stem cell using a CRISPR/Cas system for the purposes of treating β-thalassemia, with the teachings of Liu et al., wherein Liu teaches a composition comprising a cationic lipid and a pre-annealed complex comprising Cas9 protein and a gRNA, wherein the composition is capable of delivering the Cas9 protein to the interior of a cell. The skilled artisan would have found it prima facie obvious to use the CRISPR-Cas system of Liu to treat β-thalassemia, as taught by Conway, because proteins do not require transcription and translation, and can directly provide the desired therapeutic functionality.
Moreover, one of ordinary skill in the art would have looked to the teachings of Negre as Negre et al. relate to improved gene therapy compositions for expanding hematopoietic cells. The skilled artisan would have looked to the teachings of Hoge et al. as Hoge teaches methods of delivering CRISPR modified cells in vivo. Further, one of ordinary skill in the art would have found it prima facie obvious to include multiple nuclear localization signals in the Cas9 protein as Zhang teaches wild-type Cas9 does not localize into the nucleus without including multiple NLSs.
Thus, the teachings of the cited prior art in the obviousness rejection above provide the requisite teachings and motivations with a clear, reasonable expectation. The cited prior art meets the criteria set forth in both Graham and KSR.
Therefore, the claimed invention, as a whole, was clearly prima facie obvious.
Applicant’s Arguments/ Response to Arguments
Applicant argues: Conway allegedly teaches CRISPR-Cas9 modification of HSCs for treating conditions like β-thalassemia using viral vectors and nucleic acid delivery approaches. However, Conway does not teach or suggest lipid nanoparticle delivery of pre-annealed Cas9 protein:sgRNA complexes. Indeed, Conway's disclosure is directed to nuclease-encoding nucleic acids delivered via viral vectors or electroporation, not pre-assembled protein complexes delivered via lipid nanoparticles. See Conway at [0024] (describing "genetically modified HSCs" and "HSCs edited by treatment with a nuclease").
In Response: Applicant’s arguments have been fully considered, but are not found persuasive. Examiner clearly notes at para. 10 above that Conway failed to teach a particle comprising pre-annealed complex comprising CRISPR-Cas9 protein and one or more single guide RNA molecules.
Applicant argues: Liu describes cationic lipid-mediated delivery of proteins, including Cas9, but only to highly permissive, easy-to-transfect cell types. Specifically, Liu's working examples demonstrate protein complex delivery only to mouse embryonic stem cells (mESCs) at [0239] and U2OS osteosarcoma cells (a cancer cell line) at [0258]. The Examiner's statement that Liu teaches delivery to "stem cells, progenitor cells, and blood cells" (Office Action 26) mischaracterizes Liu's actual disclosure. The cited passage at Liu [0098] is a generic, prophetic list of "suitable cells" that states: "Suitable cells and cell types for delivery of functional effector proteins .. .include, but are not limited to, human cells, mammalian cells, T-cells, neurons, stem cells, progenitor cells, blood cells ... " This broad statement provides no actual demonstration, data, or enabling disclosure for primary CD34+ HSCs.
A person of ordinary skill in the art would recognize that mouse embryonic stem cells are fundamentally different from primary human CD34+ HSCs in several critical respects. Mouse ESCs are highly proliferative with open chromatin architecture and readily take up foreign materials via endocytosis. Moreover, mESCs are cultured continuously and are adapted to in vitro conditions. In contrast, primary CD34+ HSCs are quiescent (non-dividing) cells with closed chromatin, are notoriously resistant to transfection by lipid-mediated methods, and are difficult to maintain ex vivo as they lose sternness upon culture. Similarly, U2OS cells are an immortalized osteosarcoma cell line with fundamentally altered membrane properties that readily take up lipid based reagents, making them non-representative of primary, non-transformed human cells.
In Response: Applicant’s arguments have been fully considered, but are not found persuasive. MPEP 2121 states that when the reference relied on expressly anticipates or makes obvious all of the elements of the claimed invention, the reference is presumed to be operable. Once such a reference is found, the burden is on applicant to rebut the presumption of operability. Applicant has not provided any evidence that HSCs, which are a specie of the “blood cells” recited in Liu, would be inoperable in the method of Liu.
Applicant argues: The Examiner's characterization of Negre is not supported by the actual disclosure. The Examiner states that "Negre specifically teaches modification of CD34+, CD59+, Thyl/CD90+, CD38lo/-, C-kit/CDll7+, and Lin(-) HSCs with a lipid-based delivery system."
However, Negre does not teach this. Negre paragraph [0318] is a generic, prophetic statement listing potential delivery vehicles: "the compositions of the present invention may be formulated for delivery either encapsulated in a lipid particle, a liposome, a vesicle, a nanosphere, a nanoparticle or the like." This is a laundry list of potential delivery modalities with no specificity, no formulations, no protocols, no working examples, and no data. Even accepting that Negre mentions liposomes as a potential delivery option, Negre does not teach or suggest lipid-mediated delivery of pre-annealed Cas9 protein:sgRNA complexes to primary CD34+ hematopoietic stem cells. Negre's disclosure is directed entirely to gene therapy using viral vectors and nucleic acid constructs, not protein delivery. See Negre at [0289] (describing lentiviral vectors and "ex vivo protein expression").
In Response: Applicant’s arguments have been fully considered, but are not found persuasive. MPEP 2121 states that when the reference relied on expressly anticipates or makes obvious all of the elements of the claimed invention, the reference is presumed to be operable. Once such a reference is found, the burden is on applicant to rebut the presumption of operability. Moreover, Examiner did not cite Negre for teaching a lipid-mediated delivery of pre-annealed Cas9 protein:sgRNA complexes to primary CD34+ hematopoietic stem cells. Neither did the Examiner cite Negre for teaching protein delivery. Protein delivery via liposomes was/is taught in Liu. Negre was cited for teaching delivery of formulations in liposomes to HSCs.
Applicant argues: Hoge allegedly teaches liposomal formulations with cholesterol, PEG-c-DMA, and cationic lipids for delivering CRISPR components, but Hoge is directed to mRNA delivery (encoding Cas9), not pre-annealed Cas9 protein:sgRNA complex delivery. See Hoge at [0741][ 0743] (describing in vivo delivery of "FLAG-Cas9 Cong mRNA" formulated in lipid nanoparticles ). Hoge does not teach protein complex delivery to primary HSCs. Zhang allegedly teaches PCSK9 targeting, SpCas9/SaCas9 variants, multiple NLSs, and catalytic domain mutations, but does not teach or suggest lipid nanoparticle delivery or delivery to primary HSCs.
In Response: Applicant’s arguments have been fully considered, but are not found persuasive. Note that Hoge was not cited for teaching pre-annealed Cas9 protein:sgRNA complex delivery. Rather, Hoge was cited as Hoge teaches a liposome formulation comprising 48% cholesterol, 2% PEG-c-DMA, and 30% cationic lipid. Hoge teaches the suitability of this liposome formulation in delivery CRISPR components.
Applicant’s arguments: A critical fact emerges from reviewing all the cited references: not one of them demonstrates lipid-mediated delivery of pre-annealed protein:sgRNA complexes to primary CD34+ hematopoietic stem cells. This is not a coincidence-it reflects the state of the art as of 2014. The Examiner dismisses certain prior art discussing the difficulty of HSC modification, stating these references "nearly predate the effective filing date of the instant application (2014) by 10 years" Office Action 24. However, this observation actually supports Applicant's position. If lipid-mediated protein complex delivery to primary HSCs was routine and predictable by 2014 the Examiner should readily be able to cite references from 2010-2014 demonstrating such delivery with working examples and data.
Instead, the Examiner cites Gul-Uludag (2012) for "cationic liposome-mediated CXCR4
gene delivery into hematopoietic stem/progenitor cells" Office Action 24. But Gul-Uludag teaches plasmid DNA delivery-a fundamentally different cargo from pre-annealed protein: RNA complexes. DNA and protein :RNA complexes differ in size and molecular weight, surface charge density and distribution, conformational flexibility, interaction with lipid formulations, mechanism of endosomal escape, and intracellular trafficking. A teaching of DNA delivery does not render obvious protein: RNA complex delivery. The Examiner has not identified any reference teaching lipid-mediated protein: RNA complex delivery to primary HSCs. The absence of any reference between 2005 and 2014 teaching successful lipid-mediated protein complex delivery to HSCs demonstrates the technical difficulty and unpredictability, not that the problem was solved.
In Response: With respect to Gul-Uludag, it is critical to note that Examiner provided this reference solely in response to Applicant’s argument that “..despite extensive research efforts, lipid-based transfection consistently failed or was sub-optimal in HSCs compared to other delivery techniques.” Examiner cited Gul-Uludag et al. as they teach cationic liposome-mediated CXCR4 gene delivery into hematopoietic stem/progenitor cells (Title).
Furthermore, Applicant’s arguments regarding working examples and data are confusing in view of Applicant’s own specification. Indeed, at para. 421 of the PgPub, the specification teaches twenty different particle formulations were generated and tested for CRISPR-Cas9 delivery efficiency into cells. Note that these twenty formulations read on the claimed particle in claim 1. However, out of the 20 formulations, it appears that 17 failed. Moreover, none of the 3 formulations indicated as successful by the specification are specifically claimed. Applicant cannot argue that the prior art failed to successfully teach lipid-mediated protein complex delivery to primary HSCs while the breadth of the claimed invention embraces 17 formulations that by Applicant’s own admission, failed. In order to advance prosecution, Examiner suggests Applicant amend the claims such that they are drawn to the formulations that were successful in mediating protein complex delivery to primary HSCs.
Applicant argues: KSR rationale A requires predictable results when combining known elements. To find obviousness under this rationale, the Examiner must establish that a person of ordinary skill would have a reasonable expectation of success in combining the teachings. Here, the record is devoid of any evidence that lipid-mediated protein:sgRNA complex delivery to primary CD34+ HSCs would have been predictable. No reference demonstrates this delivery modality in primary HSCs. demonstrations in mESCs and U2OS cells do not establish predictability for primary HSCs, which are biologically distinct. Negre provides no enabling disclosure, data, or guidance. The Examiner's own cited art (Gul-Uludag 2012) teaches DNA delivery, not protein complex delivery.
In Response: Applicant’s arguments have been fully considered, but are not found persuasive. MPEP 2143.02 III teaches obviousness does not require absolute predictability, but at least some degree of predictability is required. In this regard, each element of the claimed invention is taught by the cited prior art. Therefore, a reasonable expectation of arriving at the claimed invention, as elaborated upon above, is present.
Applicant argues: KSR rationale G requires that the prior art contain a teaching, suggestion, or motivation to combine the references in the manner claimed. The Examiner's reasoning appears to be based on impermissible hindsight. The Supreme Court has cautioned that "the claimed invention must be obvious in light of the existing art at the time of the invention rather than obvious in light of what came later" Graham v. John Deere Co., 383 U.S. 1, 35-36 (1966). Here, the Examiner appears to be using Applicant's
In Response: In response to applicant's argument that the examiner's conclusion of obviousness is based upon improper hindsight reasoning, it must be recognized that any judgment on obviousness is in a sense necessarily a reconstruction based upon hindsight reasoning. But so long as it takes into account only knowledge which was within the level of ordinary skill at the time the claimed invention was made, and does not include knowledge gleaned only from the applicant's disclosure, such a reconstruction is proper. See In re McLaughlin, 443 F.2d 1392, 170 USPQ 209 (CCPA 1971).
Because Applicant’s arguments were not found persuasive, the rejection is maintained.
Authorization to Initiate Electronic Communications
The examiner may not initiate communications via electronic mail unless and until applicants authorize such communications in writing within the official record of the patent application. See M.P.E.P. § 502.03, part II. If not already provided, Applicants may wish to consider supplying such written authorization in response to this Office action, as negotiations toward allowability are more easily conducted via e-mail than by facsimile transmission (the PTO's default electronic-communication method). A sample authorization is available at § 502.03, part II.
Conclusion
No claim is allowed.
THIS ACTION IS MADE FINAL. Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any extension fee pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
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/TITILAYO MOLOYE/Primary Examiner, Art Unit 1632